Flashcards in Renal endocrinology Deck (69)
What is the action of parathyroid hormone?
Increase blood concentrations of calcium
How does parathyroid hormone carry out its function?
- Stimualtes production of calcitriol in kidney
- Facilitates mobilisation of calcium and phosphate from bone
- Maximise tubular reabsorption of calcium within teh kidney
What is the action of calcitonin?
Decrease blood calcium
How does calcitonin carry out its function?
- Suppress renal tubular reabsorption of calcium
- Inhibits bone resorption
Why are calcium and phosphorous considered together?
- React in opposite ways
- As calcium increases, phosphate falls and vice versa
- Can bind together
How are calcium and phosphorous linked to iron?
- Are all divalent ions, so need ion transported in order to be absorbed from GI tract
- Compete for these transporters
- I.e. excess calcium in diet leads to iron deficiency
Describe the actions of magnesium in the body
- Enzyme cofactor
- Needed for regulation of blood glucose, production of energy and protein, nerve transmission, muscle contraction, bone and cel formation
What is unusual about magnesium in ruminants?
- Is absorbed from rumen
- In otehers is absorbed from small and large intestine
What condition is caused by low magnesium intake? What are the signs?
- Hypomagnesaemic tetany
- Aka Grass Staggers
- Often cows
- Weakness, muscle cramps, tremors
Why does renal failure often lead to derangements of calcium and phosphorous?
- Calcitriol synthesised in kidney
- No calcitriol = no absorption of calcium from intestine = deficiency
- Tubular reabsorption of calcium in the kidney
Why does bone demineralisation occur in renal failure?
- Increased PTH to increase blood calcium
- No calcitriol to feedback to stop PTH production
- PTH continues to be produced, causes bone resorption
What is RAAS?
Renin angiotensin aldosterone system
What are the mechanisms of autoregulation of renal blood flow?
- Myogenic feedback
- Tubuloglomerular feedback
Describe myogenic feedback in high bood pressure
- Increased renal blood flow
- Stretch vascular smooth muscle in afferent arteriole
- Calcium entry, release of more Ca from internal stores
- Automatic constriction of afferent arteriole to reduce glow to glomerulus and decrease GFR
Describe myogenic feedback low blood pressure
- Reduced renal blood flow
- Reduced stretch of vascular smooth muscle
- Automatic vasodilation of afferent to increase flow to glomerulus (increase GFR)
Why is the renal myogenic response considered to be pre-renal?
Controls the blood going into the renal corpuscle
Describe the mechanisms of tubuloglomerular feedback
- Signal from distal tubule to glomerulus to reciprocally alter filtration
- Decrease flow rate in ascending LoH = increase GFR in same nephron
- Also related to NaCl levels in tubular fluid
Describe the effect of NaCl in tubuloglomerular feedback
- NaCl low, cells at macula densa generate less adenosine
- Stimulates decreased intracellular Ca in VSMC = afferent vasodilation
- Reverse with high NaCl
What is the action of prostaglandins and nitric oxide on the afferent arteriole?
Vasodilate (to protect against severe vasoconstriction)
What occurs in acute heamorrhage?
- Intrinsic mechanisms of kidney (myogenic and tubuloglomerular feedback)
- Extrinsic mechansms e.g. sympathetic system, angiotensin II, endothelin, prostaglandins, nitric oxide
- Main aim is to maintain pressure to brain, massive total peripheral vasoconstricton
How does the kidney control blood pressure?
- Water balance (blood volume directly impacts blood pressure)
- Hormonal (stimulation of RAAS)
- Macula densa
- Acts to monitor blood pressure and stimulate hormonal systems, since recevies 20% of cardiac output and has high perfusion
What are the components of the RAAS and where are these produced what is their stimulation?
- Renin: kidney, low perfusion
- Angiotensin: liver, in response to renin
- Aldosterone: adrenal gland cortex in response to Ang II
Describe how the RAAS works
- Low perfusion sensed by kidney
- Release of renin
- Catalyses conversion of angiotensinogen to angiotensin I
- Angiotensin I to angiotensin II using ACE from lungs and endothelial cells
- Angiotensin II to adrenal cortex to stimulate aldosterone secretion
- Aldosterone acts on kidney to increase Na retention
What are the actions of angiotensin II?
- Increase sympathetic activity
- Increase Na, Cl reabsorption, K_ excretion and thus H2O retention
- Stimulate aldosterone secretion
- Arteriolar vasoconstriction to increase blood pressure
- Stimulate ADH secretion to increase collecting duct reabsorption of H2O
What is the action of RAAS in relation to blood pressure?
- Stabilise blood pressure rapidly
- Enables variable salt intake whilst maintaining ECF volume and thus arterial pressure
What is the function of the macula densa?
- Senses distal tubule and afferent/efferent arterioles
- Increase or decrease nerve firing and flow rate in response
Describe the overall effect of RAAS
- Loss of blood volume > redcued ECF > BP falls > renal flow falls > tubular flow decreased > less NaCl to macula densa > stimualtes renin from juxtaglomerular apparatus > increased intrarenal and systemic Ang II > increase systemic and intrarenal resistance > support continued filtration despite reduced RBF adn increased peripheral vascular resistance
How does angiotensin II exert its actions in the renal tubules as a whole?
Insertion of Na+ channels in renal tubules via AT1 receptors
How does angiotensin II exert its actions in the proximal tubule?
- Inserts apical Na+/H+ exchanger
- Inserts basolater Na+3(HCO3-) and Na+/K+ ATPase